Profiles of type-II pneumocytes in rats inoculated ...

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Title Profiles of type-II pneumocytes in rats inoculated intratracheally with bacterial lipopolysaccharide
Author(s) Alphonso Lopez, M. Albassam, S. Yong, A. Sharma, L. E. Lillie, M. G. Prior
Journal American Journal of Veterinary Research
Date 1987
Volume 48
Issue 10
Start page 1534
End page 1539
Abstract Ultrastructural and morphometric profiles of type-II pneumocytes (P-II) were investigated in rats killed 18 or 24 hours after a single intratracheal inoculation of bacterial (Escherichia coli) lipopolysaccharide (LPS). Inoculation with LPS induced pulmonary injury and inflammation, as measured by increased lactate dehydrogenase and alkaline phosphatase activities and increased numbers of polymorphonuclear neutrophils in fluid collected by bronchoalveolar lavage. Marked ultrastructural changes and desquamation of a few P-II developed at the time of high activity of lactate dehydrogenase and alkaline phosphatase in bronchoalveolar lavage fluid. Ultrastructural changes included swollen mitochondria and localized cisternal dilatation of the endoplasmic reticulum in which was contained membrane-bound homogenous material of medium electron density. Twenty-four hours after LPS inoculation, point-count stereologic analysis and digitizing morphometry revealed >50% increase in P-II size. Changes in cell size corresponded with ultrastructural finding of swollen cells. Results obtained by point-count stereologic analysis and digitizing morphometry were highly correlated (r=0.95). Lamellar bodies (LB) comprised 12 to 15% of P-II volume. Volume density and number of LB remained unaltered in LPS-injured P-II, and evidence of accelerated release of LB was not detected after LPS inoculation. Exudated polymorphonuclear neutrophils and pulmonary alveolar macrophages were involved actively in the phagocytosis of LB originating from necrotic and desquamated P-II. On the basis of measurement of enzyme activity (enzymes released into the bronchoalveolar space), considerable ultrastructural alterations developed in P-II when maximal LPS-induced pulmonary cell injury took place.

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